Since the apparition of new technologies permitting the precise characterization of microorganisms, studies involving microbiotas’ influence swarmed in the literature. It has also brought evidences to raise the emerging concept that the lung is not a sterile compartment and possesses its own microbiota. It has been shown that the lung microbiota could be altered in patients suffering of respiratory diseases, such as asthma or bronchiolitis induced by respiratory syncytial virus (RSV). However, we still don’t know if it is pathologies that influences the dysbiosis or the reverse. Despite this fundamental question, we know that microbiota is able to affect the immune response. But, the manner by which this phenomenon occurs remains elusive. First, using lung explants from specific pathogen free (SPF) and germ-free (GF) mice exposed to Toll-like receptors (TLRs) ligands or RSV, we show a higher production of pro-inflammatory cytokines, notably IL-6 and TNF by lung explants from GF mice compared to SPF mice. These data suggest that microbiota educates innate immune response in lung by reducing pro-inflammatory pathways. We have also observed a more abundant expression of TLR4 in the lungs of GF mice compared to SPF mice, which could predispose the innate immune system of GF mice to react strongly to environmental stimuli. In this context, the microbiota seems to modulate innate immune receptors expression. Not only these data partially explain how the microbiota educates the immune system, but they also allow to strengthen the emerging concept of immunomodulation by probiotics bacteria to prevent respiratory pathology development.